文章摘要

乙醇脱氢酶 1C 基因多态性与酒精性肝硬化易感性的 Meta 分析

作者: 1何 晶晶, 1张 岭漪, 2张 亚武, 2张 有成
1 兰州大学第二医院 肝病科,甘肃 兰州 730030
2 兰州大学第二医院 普通外科,甘肃 兰州 730030
通讯: 张 有成 Email: hanxw2016@126.com
DOI: 10.3978/.2018.07.011
基金: 甘肃省兰州市科技计划资助项目(2012-1-29)。

摘要

目的:采用 Meta 分析的方法定量评价乙醇脱氢酶 1C(ADH1C)基因多态性与酒精性肝硬化(ALC)易感性的关系。
方法:计算机检索多个国内外数据库,搜索相关的病例对照研究,检索时间截止 2017 年 10 月。采用Stata 12.0 软件进行统计分析。
结果:共纳入 14 篇病例对照研究,其中病例组 1 457 例,对照组 2 715 例。全组分析结果显示,在等位基因模型(OR=1.17,95% CI=1.02~1.34,P=0.013)、 杂合子模型(OR=1.39,95% CI=1.16~1.66, P=0.035)、 纯合子模型(OR=1.27,95% CI=1.02~1.58,P=0.036) 及显性模型(OR=1.37,95% CI= 1.16~1.63,P=0.027)中 ALC 的发病风险明显升高,而在隐性模型(OR=1.19,95% CI=0.98~1.44, P=0.052)中 ALC 发病风险无明显变化。亚组分析结果显示,亚洲人群在等位基因模型(OR=1.43,95% CI= 1.07~1.90,P=0.037)、杂合子模型(OR=1.53,95% CI=1.14~2.04,P=0.034)、纯合子模型(OR=1.52, 95% CI=1.05~2.18,P=0.036)、显性模型(OR=1.52,95% CI=1.14~2.03,P=0.039)及隐性模型(OR=1.51, 95% CI=1.08~2.11,P=0.016)中 ALC 发病风险均升高,而高加索人群仅在杂合子模型(OR=1.31, 95% CI=1.04~1.64,P=0.038) 及显性模型(OR=1.30,95% CI=1.05~1.60,P=0.022) 中 ALC 发病风险升高。
结论:ADH1C 基因多态性与 ALC 的易感性密切相关,携带突变杂合子、突变纯合子基因型及突变等位基因型的人群罹患 ALC 的风险可能增加。
关键词: 肝硬化,酒精性;醇脱氢酶;多态性,单核苷酸;Meta 分析

Meta-analysis of relationship between alcohol dehydrogenase 1C polymorphisms and susceptibility to alcoholic liver cirrhosis

Authors: 1Jingjing HE, 1Lingyi ZHANG, 2Yawu ZHANG, 2Youcheng ZHANG
1 Department of Liver Disease, the Second Hospital, Lanzhou University, Lanzhou 730030, China
2 Department of General Surgery, the Second Hospital, Lanzhou University, Lanzhou 730030, China

CorrespondingAuthor:Youcheng ZHANG Email: hanxw2016@126.com

Abstract

Objective: To assess the relations of alcohol dehydrogenase 1C (ADH1C) gene polymorphisms with the susceptibility to alcoholic liver cirrhosis (ALC) through Meta-analysis.
Methods: The relevant case-control studies were retrieved by searching several national and international databases from their inception to October 2017. Statistical analyses were performed by using Stata 12.0 software.
Results: A total of 14 case-control studies were included, involving 1 457 patients in case group and 2 715 subjects in control group. Results of the entire group showed that the risk of ALC was significantly increased in allele model (OR=1.17, 95% CI=1.02–1.34, P=0.013), heterozygous model (OR=1.39, 95% CI=1.16–1.66, P=0.035), homozygous model (OR=1.27, 95%CI=1.02–1.58, P=0.036) and dominant model (OR=1.37, 95% CI=1.16–1.63, P=0.027), but had no significant change in recessive model (OR=1.19, 95% CI=0.98–1.44, P=0.052). Results of subgroup analysis showed that the risk of ALC among Asian populations was increased in allele model (OR=1.43, 95% CI=1.07–1.90, P=0.037), heterozygous model (OR=1.53, 95%CI=1.14–2.04, P=0.034), homozygous model (OR=1.52, 95% CI=1.05–2.18, P= 0.036), dominant model (OR=1.52, 95% CI=1.14–2.03, P=0.039) and recessive model (OR=1.51, 95% CI=1.08–2.11, P=0.016), while an increased risk of ALC was only found in heterozygous model (OR=1.31, 95% CI=1.04–1.64, P=0.038) and dominant model (OR=1.30, 95% CI=1.05–1.60, P=0.022) among Caucasian populations.
Conclusion: ADH1C gene polymorphism is closely related to ALC susceptibility, and those with heterozygous mutation, homozygous mutation and mutant allele genotype may have increased risk of ALC.
Keywords: Liver Cirrhosis Alcoholic; Alcohol Dehydrogenase; Polymorphism Single Nucleotide; Meta-Analysis